We found that moderate to severe LV diastolic dysfunction was present in 10% of outpatients with CHD who had no systolic dysfunction or history of HF. The presence of asymptomatic moderate to severe LV diastolic dysfunction predicted a more than sixfold increased risk of incident HF and an almost fourfold increased risk of death from heart disease. The increased risk of cardiovascular events associated with asymptomatic LV diastolic dysfunction was similar to that observed for patients with known HF.2
Our results highlight the importance of asymptomatic LV diastolic dysfunction and raise the possibility that patients with LV diastolic dysfunction may benefit from more aggressive therapy to prevent or delay the development of clinical HF.
In this study, we sought to define the prevalence of asymptomatic LV diastolic dysfunction in patients with stable CHD and examine the prognosis of LV diastolic dysfunction in patients without systolic dysfunction or history of HF. One previous study examined the association of LV diastolic dysfunction with cardiovascular outcomes in patients without known heart disease,4
but the prevalence and prognosis of asymptomatic LV diastolic dysfunction in outpatients with stable CHD is unknown. Because patients with CHD are at high risk of developing HF,11
this group represents a relevant target population for which closer follow-up and earlier interventions to prevent HF might be considered.
We found that asymptomatic moderate to severe LV diastolic dysfunction predicted hospitalization for HF and death from heart disease at rates similar to those observed with clinically overt HF. Because LV diastolic dysfunction did not predict subsequent myocardial infarction, the association of LV diastolic dysfunction with death from heart disease was likely caused by the interim development of HF. We considered the possibility that greater LV mass, lower LV ejection fraction, more inducible ischemia, or lower creatinine clearance might explain the observed association between LV diastolic dysfunction and HF. However, even after adjusting for these factors, the association of LV diastolic dysfunction with HF remained strong.
In addition to the 10% prevalence of moderate to severe LV diastolic dysfunction in our patients, we found a 24% prevalence of mild LV diastolic dysfunction. Thus, the overall prevalence of LV diastolic dysfunction was 34%. Bursi et al2
found that LV diastolic dysfunction was present in 44% of community-dwelling patients with HF. The lower prevalence of LV diastolic dysfunction in our study is likely explained by our study population, which consists of patients with stable CHD, but no history of HF. Although impaired relaxation predicted subsequent myocardial infarction and death from heart disease in unadjusted analyses, this association was no longer significant after adjusting for potential confounding variables. This indicates that other factors associated with impaired relaxation, such as LV hypertrophy or inducible ischemia, may have been responsible for the increased rate of adverse events. This is supported by higher incidences of LV hypertrophy and inducible ischemia in the impaired-relaxation group compared with normal patients.
American College of Cardiology/American Heart Association guidelines for the evaluation and management of chronic HF recommend specific therapies for each of 4 stages in the evolution of HF.12
In adults at high risk of HF, but without structural heart disease or symptoms of HF (stage A), the guidelines recommend aggressive risk-factor reduction, including smoking cessation, exercise, and treatment of hypertension. In patients with structural heart disease, but without symptoms of HF (stage B), the guidelines specifically recommend therapy with angiotensin-converting enzyme inhibitors and β
blockers. In our study patients with CHD, the presence of asymptomatic LV diastolic dysfunction appeared to differentiate between those with stage A HF (at risk of HF, but without structural heart disease or symptoms of HF) and those with stage B HF (structural heart disease, but without symptoms of HF). Thus, the presence of LV diastolic dysfunction identifies a subgroup of patients who may benefit from more aggressive afterload reduction with angiotensin-converting enzyme inhibitors and β
blockers. However, although treatments for asymptomatic systolic dysfunction have been well established, therapies for asymptomatic LV diastolic dysfunction have yet to be evaluated in clinical trials.